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Flashcards in 30 Pathology of the Colon Deck (25):
1

Quick review of the colon (p.2-3)

  • Anatomy Normal colon 
    • measures/
    • divided into/
    • two sharply angulated junctions, 
  • Histology 
    • The wall of the colon consists of/
  • Physiology and functions 
    •  

  • Anatomy Normal colon
    • measures about 90 to 125 cm in length
    • divided into the cecum, ascending colon, transverse colon, descending colon, sigmoid colon and rectum.
    • two sharply angulated junctions,
      • hepatic flexure,
      • splenic flexure.
  • Histology
    • The wall of the colon consists of mucosa, muscularis mucosae, submucosa, muscularis propria, and serosa.
  • Physiology and functions
    • to absorb any remaining water and electrolytes from the chyme,
    • to continue moving the waste material along its way,
    • to store the waste material until it is time for it to be evacuated.

2

Acute abdomen (p.6)

  • defined generally as
  • General causes of acute abdomen 

  • defined generally as an intraabdominal process causing severe pain and often requiring surgical intervention.
  • General causes of acute abdomen
    • inflammatory, 
    • mechanical,
    • neoplastic,
    • vascular,
    • traumatic, 
    • congenital defects. 

3

Acute appendicitis (p.9-10)

  • Clinical Features: 
    • ?
    • develops/
    • causes/
  • Pathogenesis: 
    • Both appendiceal calculi and fecalith
    • Fecaliths/
    • Acute inflammation/
    • Secretions/
    • Once bacterial infection established/
  • Grossly, 
    • the appendix is/
    • Obstruction/
    • The most common causes of obstruction
  • Histologically, 
    • acute inflammation varies from/
    • Acute inflammation may extend into/

  • Clinical Features:
    • one of the commonest acute surgical emergencies and most readily curable inflammatory diseases of the GI tract.
    • develops at any age with a peak incidence in the second and third decades.
    • causes acute periumbilical, colicky pain, vomiting, or localized jejunal ileus.
      • Fever and leukocytosis develop with the onset of peritoneal inflammatory signs in the right lower quadrant.
  • Pathogenesis:
    • Both appendiceal calculi and fecalith may obstruct the appendiceal lumen.
    • Fecaliths can be visualized radiographically in 7 to 12% of adults with acute appendicitis, depending on their mineral content.
    • Acute inflammation occurs when the appendix become obstructed.
    • Secretions accumulate under pressure behind the obstruction and normal peristaltic drainage fails to occur.
    • Once bacterial infection established, vascular occlusion, gangrene, and perforation develop quickly.
  • Grossly,
    • the appendix is edematous and swollen, with fibrinous and purulent exudate covering the serosal surface.
    • Obstruction of the lumen can be seen in 30 to 40% of cases.
    • The most common cause of obstruction is fecalith, followed by lymphoid hyperplasia, carcinoid tumor, and worms.
  • Histologically,
    • acute inflammation varies from mild to severe, with necrosis and complete destruction of the entire appendiceal wall.
    • Acute inflammation may extend into the surrounding fat in severe cases and produce periappendicitis.

4

Acute diverticulitis (Diverticular disease) (p.12-13)

  • Diverticula
  • prevalence
  • Decreased luminal fiber and lower stool volume require/
  • The increased segmentation generates/
  • The colonic wall is weakest where/
    • 10 to 25 percent of patients/
  • Complications of diverticular disease

  • Diverticula are acquired pouches of mucosa and submucosa which herniate through the muscular layers of the colon.
  • The prevalence of diverticular disease in Western countries abruptly increased 30 years after the introduction of grain milling factories, which greatly decreased the fiber content in grain.
  • Decreased luminal fiber and lower stool volume require more colonic segmentation to propel fecal material forward.
  • The increased segmentation generates greater intraluminal pressures predisposing to diverticular disease.
  • The colonic wall is weakest where nutrient or penetrating arteries pierce the muscularis propria; this is where the diverticula typically form.
  • Most people with diverticulosis remain asymptomatic, only to be diagnosed incidentally.
    • 10 to 25 percent of patients become symptomatic, usually due to development of diverticular inflammation (diverticulitis).
  • Complications of diverticular disease include bleeding, free perforation, fistula formation, peritonitis, obstruction, and peri-diverticular abscesses.

5

Ischemic bowel disease (p.15)

  • The colon receives blood from/
    • In ischemia, the colon receives/
    • watershed areas
  • The three main causes 
  • Mimcs
  • Three clinical types of ischemic injury develop in the colon: 
    • a low-grade transient reversible form/
    • a high-grade fulminant form/
    • a chronic persistent/recurrent form/

  • The colon receives blood from the superior and inferior mesenteric arteries, rectal arteries, and branches of the internal iliac and pudendal arteries.
    • In ischemia, the colon receives less blood than is necessary to maintain its structure and function.
    • there are several weak points in the colonic vasculature, which has been named “watershed areas.”
      • the splenic flexure, or Griffith’s point
      • the rectosigmoid region, or Sudeck’s point.
  • The three main causes
    • vascular occlusion due to formation of atheroma, thrombi, emboli, or vasculitis
    • nonocclusive ischemia due to hypotension as seen in shock and ventricular failure
    • mechanical vascular compression.
  • Mimcs
    • Oral contraceptive may cause similar histological changes due to its thrombogenic property.
    • Other mimic include enterohemorrhagic E. coli and C. difficile infections.
  • Three clinical types of ischemic injury develop in the colon:
    • a low-grade transient reversible form that usually confined to the mucosa or submucosa and followed by spontaneous healing;
    • a high-grade fulminant form that progressively destroys all layers of the bowel wall, usually with catastrophic consequences, including transmural necrosis and perforation;
    • a chronic persistent/recurrent form that lasts for months and extends into the bowel wall and causes fibrosis and stricture.

6

Ischemic bowel disease (p.16-19+22-23)

  • Grossly,
    • ischemia often shows/
    • This is typically accompanied by/
    • most common site for ischemic lesions of the colon
    • Healed ischemic lesions may form/
  • Histologically,
    • the acute early ischemic lesions show/
      • recovery at this stage
    • Later, the histology is characterized by/
      • recovery at this stage
    • The chronic phase of ischemia may be more difficult to diagnose because the only histologic finding may be/

  • Grossly,
    • ischemia often shows geographic areas of ulceration with pseudomembranes.
    • This is typically accompanied by marked submucosal edema, a finding that gives rise to “thumbprinting” pattern seen in barium enemas.
    • Watershed areas around the splenic flexure are the most common site for ischemic lesions of the colon; however, nearly any site can be ischemic.
    • Healed ischemic lesions may form strictures that mimic Crohn’s disease.
  • Histologically,
    • the acute early ischemic lesions show patchy or diffuse areas of hemorrhagic necrosis of the superficial mucosa without associated inflammation or the involvement of the deeper portions of the colon.
      • At this stage, the changes are reversible and complete recovery is possible if the blood flow is restored.
    • Later, the histology is characterized by complete necrosis of the mucosa with secondary bacterial infection, leading to ulceration, perforation and associated peritonitis.
      • Complete recovery is unlikely in this stage and surgery may be required.
    • The chronic phase of ischemia may be more difficult to diagnose because the only histologic finding may be areas of submucosal fibrosis and stricture that are rather nonspecific.

7

Infectious colitis: Colonic causes of diarrhea:
Enterohemorrhagic Escherichia coli

  • Enterohemorrhagic colitis 
    • results from/
    • what contribute to the pathogenicity
    • A unique plasmid-encoded fimbrial adhesin facilitate/
      • As a result/
    • These toxins 
      • damage/
      • mediate/
    • Shiga toxin-producing E. coli associate with/
    • preventive measures
    • Patients with colitis develop/
  • The histologic features demonstrate/
    • Features associated with ischemic damage include/
      • The ischemia leads to/
    • Histologic features associated with an infectious pattern include/

  • Enterohemorrhagic colitis
    • results from colitis due to Shiga toxin-producing E. coli.
      • O157:H7 is one strain of Shiga toxin-producing E. coli that is most commonly isolated in the United States.
    • Two similar but distinct bacterial cytotoxins (Shiga-like toxins I and II) contribute to the pathogenicity.
    • A unique plasmid-encoded fimbrial adhesin facilitate the adherence of E. coli 0157:H7 to the intestinal mucosa.
      • As a result, entero-hemorrhagic E. coli do not invade the epithelium but rather adhere to the luminal surface where they elaborate a toxin that is then absorbed.
    • These toxins
      • damage the vascular endothelium of the kidney and intestine
      • mediate bacillary dysentery, hemorrhagic colitis, HUS (hemorrhagic uremic syndrome) and TTP (thrombotic thrombocytic purpura).
    • Shiga toxin-producing E. coli associate with contaminated drinking water, and the consumption of hamburgers, other beef products, unpasteurized milk, cheese, pork, poultry, lamb, deer jerk, vegetables, and fruits.
    • Proper cooking is the preventive measures of choice.
    • Patients with colitis develop bloody diarrhea, severe crampy abdominal pain, and low-grade fever.
  • The histologic features demonstrate overlapping ischemic and infectious patterns due to the presence of both epithelial and endothelial injury.
    • Features associated with ischemic damage include focal marked submucosal edema, hemorrhage, and pseudomembranes.
      • The ischemia leads to extensive mucosal necrosis leaving ghost of crypts with underlying neutrophilic infiltrates.
    • Histologic features associated with an infectious pattern include a prominent neutrophilic infiltrate within the crypts, lamina propria, and adherent pseudomembranes.

8

Infectious colitis: Colonic causes of diarrhea:
Clostridium difficile (p.28-30)

  • antibiotic-associated colitis
  • common symptoms
  • diagnostic
  • Grossly/
  • Histologically/

  • Some individuals may develop colitis (antibiotic-associated colitis) following the use of various antibiotics.
    • Originally colitis was seen as a complication resulting from use of clindamycin and ampicillin,
    • now it has been noted after the use of all antimicrobial agents.
    • treatment favors the proliferation of Clostridium difficile, which is normally present in the bowel, leading to increased production of the species toxin.
  • Diarrhea and abdominal pain are common symptoms.
  • The finding of pseudomembranes through endoscopy and a positive assay to the toxin in the stool are diagnostic.
  • Grossly, pseudo-membranes are raised mucosal plaques composed of fibrin, red blood cells, neutrophils and cell debris.
  • Histologically, mucosal biopsies in early stage show areas of surface glandular drop-out and necrosis which are very similar to early ischemic changes.

9

Infectious colitis: Colonic causes of diarrhea:
Shigella (p.33)

  • Shigella
  • main victims
  • The two major clinical presentations
  • Grossly, /
  • Microscopic changes
  • recovery

  • Shigella is a nonmotile, gram-negative bacillus that penetrates the intestinal mucus layer and invades the epithelium.
  • Children are the main victims of Shigella infection.
  • The two major clinical presentations
    • watery diarrhea
    • dysenteric syndromes which include bloody mucoid stool, intense crampy abdominal pain, diarrhea, fever, nausea and vomiting.
  • Grossly,
    • the mucosa appears friable, hyperemic and ulcerated.
    • All patients have inflammation in the rectosigmoid area.
    • Serpiginous ulcers develop on the free edge of the mucosal folds oriented transversely to the long axis.
  • Microscopic changes include small aphthous ulcers, acute inflammation with neutrophilic emigration, superficial crypt abscess formation, early goblet cell depletion, edema, erythema, and mild plasma cell infiltrates.
  • Even in the case of extensive mucosal damage, recovery is usually very rapid.

10

Infectious colitis: Colonic causes of diarrhea:
Cytomegalovirus (CMV) (p.34)

  • categorized as
  • elimination
  •  incidence
  • present with/
  • diagnosis
  • In severely immunosuppressed patients, numerous CMV-infected cells are identified by the presence of/

  • categorized as primary infections, reactivation infection, and superinfections.
  • usually not eliminated from the body after primary infection.
    • persists as a low-grade chronic infection or remains in a latent state.
  • The incidence increases among newborns, organ or bone marrow transplant recipients, HIV infected persons or blood transfusion recipients.
  • present with abdominal pain, watery or bloody diarrhea, chronic hemorrhage, perforation and peritonitis.
  • The diagnosis in mucosal biopsies
  • In severely immunosuppressed patients, numerous CMV-infected cells are identified by the presence of both nuclear and cytoplasmic inclusions.
    • Viral inclusions are present both in the epithelium and stromal cells including fibroblasts and endothelial cells.
    • The absence of viral inclusions does not exclude a diagnosis of CMV.

11

Infectious colitis: Colonic causes of diarrhea:
Entameba histolytica (p.35)

  • causes/
  • involves/
  • most common symptoms
  • spread through/
  • Grossly
  • Histologically/
    • The ameba can be found
  • The most serious complication
  • Sometimes these abscesses penetrate/

  • Amebiasis is caused by a common protozoan, Entameba histolytica,
  • involves the large bowel, predominantly the cecal region.
  • Bloody diarrhea, pain, and cramp are the most common symptoms.
  • spread through contaminated food and water, although venereal transmission occurs between male homosexuals due to fecal-oral contamination.
  • Grossly, small and round ulcers are found with colonoscopy.
  • Histologically, biopsies or resection show the typical liquefaction, inflammation, and mucosal ulceration known as “ flask-like” ulcers because of broad base and narrow neck.
    • The ameba can be found in the exudate, where round trophozoites with large nuclei and ingested erythrocytes are identified.
  • The most serious complication is invasion of veins with subsequent metastasis to the liver, where an abscess may form.
  • Sometimes these abscesses penetrate the diaphragm and cause empyema and lung abscess.

12

Infectious colitis: Colonic causes of diarrhea:
Cryptosporidium (p.36)

  • Recently, the protozoan, Cryptosporidium, has been recognized as a frequent cause of colitis in immunocompromised individuals and AIDS patients, although infections may also affect immunocompetent individuals. AIDS patients, unlike immuno-competent patients, cannot clear the organisms, and so the infection often persists for the remainder of the patient’s life. Affected patients frequently have CD4 counts measuring <100 cells/mm3; they usually measure <50 cells/mm3.
  • The organisms can be recognized as clusters of spherical or oval basophilic (bluish) or golden brown bodies measuring 2 to 4 m in diameters attached to epithelial surface. They can be easily overlooked or mistaken for mucus droplets. Electron microscopy can be used to illustrate the various stages of the organisms in tissues but is not required to make the diagnosis.

13

Microscopic colitis: Noninfectious causes of colonic diarrhea:
There are patients with diarrhea who have normal appearing mucosa at endoscopy but abnormal colonic biopsies. In these patients one should be on the lookout for:
Collagenous colitis (p.39)

  • gender
  • age
  • A significant percentage of patients with collagenous colitis have a history of/
  • Symptoms
  • Collagenous colitis exhibits/
  • The histological hallmark

  • The female-to-male ratio is 10:1,
  • age range of 23 to 86 and a mean of 54 years.
  • A significant percentage of patients with collagenous colitis have a history of using NSAIDs and antibiotics.
  • Symptoms include watery, non-bloody diarrhea with up to 20 stools per day.
    • The diarrhea can last for months and decades.
    • Colicky abdominal pain occurs frequently.
  • Collagenous colitis exhibits spontaneous remission ans relapses; occasionally the disease resolve spontaneously.
  • The histological hallmark is mucosal chronic inflammation associated with a broad, continuos, hypocellular, and linear, subepithelial fibrous band immediately underneath the surface epithelium.
    • The subepithelial collagen layer measures 10 to 70 m in thickness, with a mean of 12 to 30 mcirom.
    • The thickened subepithelial layer stains light pink with PAS and blue with Masson trichrome stain.

14

Microscopic colitis: Noninfectious causes of colonic diarrhea:
There are patients with diarrhea who have normal appearing mucosa at endoscopy but abnormal colonic biopsies. In these patients one should be on the lookout for:
Lymphocytic colitis (p.41)

  • present with
  • who exhibit lymphocytic colitis
  • age and gender
  • The most distinct features

  • present with chronic watery diarrhea that can be continuous or intermittent, ranging in duration from 2 months to 25 years.
  • Up to one-third of patients with histologic evidence of gluten-sensitive enteropathy in the small bowel exhibit lymphocytic colitis.
  • This disorder occurs at all ages and equally affects both men and women.
  • The most distinct features is the presence of increased intra-epithelial lymphocytes, particularly at the luminal surface.
    • To be of diagnostic significance, the increase of T-lymphocytes must average at least 20 lymphocytes per 100 epithelial cells.
    • This threshold compares an average of 4-5 lymphocytes per 100 epithelial cells in the normal colon.

15

Idiopathic inflammatory bowel disease (IBD):
Ulcerative colitis (UC) (p.44-47+49-51)

  • Gross pathology: 
    • affects/
    • Among patients with UC/
    • characterized by/
    • the external surface of the colon appears/
    • In active UC, the mucosal surface/
    • In areas of inactive (quiescent) disease, the mucosa appears/
    • The appendix may also show/
    • worrisome for dysplasia and tumor
  • Microscopic pathology: 
    • seen in active and quiescent disease
    • In areas of active disease there is
    • Inflammatory (pseudo)polyps are composed of 

  • Gross pathology:
    • affects only the colon
      • the distal few cm of terminal ileum may be involved in an ulcerative pan-colitis (so-called “backwash ileitis”).
      • always involves the distal colon (rectum), with variable proximal continuous extension.
      • stops abruptly either at ileocecal valve or in more distal portions of the colon.
    • Among patients with UC, about 25% have only proctitis, approximately 50% have left-side colitis (up to splenic flexure), and the remaining 25% have pan-colitis (involving the entire colon).
    • primarily a mucosal disease characterized by an inflammatory reaction that remains limited to the mucosa and the superficial portion of the submucosa.
    • the external surface of the colon appears normal unless cancer or toxic megacolon has developed.
    • In active UC, the mucosal surface is diffusely congested, hemorrhagic, and friable and there may be erosion or ulceration.
    • In areas of inactive (quiescent) disease, the mucosa appears atrophic, with loss of normal pattern of folds.
      • Inflammatory polyps of varying sizes and shapes can be seen.
    • The appendix may also show active or quiescent mucosal disease.
    • Strictured areas and raised flat lesion with a velvety mucosal appearance are worrisome for dysplasia and tumor.
  • Microscopic pathology:
    • Distortion of the crypt architecture is seen in active and quiescent disease.
    • In areas of active disease there is a diffuse intense inflammatory cell infiltrate in the lamina propria, composed of lymphocytes, neutrophils and eosinophils with foci of cryptitis and crypt abscesses.
    • Inflammatory (pseudo)polyps are composed of hyperplastic mucosa with cystically dilated crypts and intense inflammation.

16

Idiopathic inflammatory bowel disease (IBD):
Ulcerative colitis (UC) (p.52+54+56)

  • Dysplasia and adenocarcinoma as a complication of ulcerative colitis: 
    • the risk of adenocarcinoma
    • Screening colonoscopy
    • Dysplasia/
      • Grossly/
      • DALM (dysplasia-associated lesion or mass)
  • Dysplasia is graded as follows:
  • Unfortunately, the cytological features of dysplasia are similar to/
  • The evaluation of dysplasia is prone to/

  • Dysplasia and adenocarcinoma as a complication of ulcerative colitis:
    • After 10 years of disease duration, the risk of adenocarcinoma sharply increases.
      • The risk of adenocarcinoma increases with the length (or extent) of the colon involved by UC.
    • Screening colonoscopy (every 1-3 years after 10 years of duration) with random biopsy is recommended by many gastroenterologists to detect dysplasia and early stage of adenocarcinoma.
    • Dysplasia is the unequivocal neoplastic epithelium confined to the basement membrane.
      • Grossly, dysplasia appears as a velvety, plaque-like area.
        • It may be isolated or multifocal.
      • It is particularly worrisome if dysplasia is associated with stricture or a mass, so-called DALM (dysplasia-associated lesion or mass) because a cancer may already develop from the pre-existing dysplasia.
  • Dysplasia is graded as follows:
    • Negative for dysplasia
    • Indefinite for dysplasia
      • Probably reactive
      • Probably dysplasia
    • Positive for dysplasia
      • Low-grade dysplasia
      • High-grade dysplasia
  • Unfortunately, the cytological features of dysplasia are similar to changes induced by active inflammation (reactive atypia).
  • The evaluation of dysplasia is prone to both intra- and inter-observer variability.
    • Sometimes, it is essential to seek a second opinion from another pathologist.

17

Idiopathic inflammatory bowel disease (IBD):
Crohn’s disease (CD) (p.61-64+66-69)

  • Gross pathology: 
    • affect 
    • There may be/
    • The mucosa may exhibit/
  • Microscopic pathology: 
    • In areas of active disease, there is transmural inflammatory cell infiltrate composed of/
    • There is marked mucosal architectural distortion with/
    • The submucosa and muscularis propria are/
    • often present
    • seen in all layers of the bowel wall and in mesenteric lymph nodes

  • Gross pathology:
    • can affect any part of the GI tract.
      • Affected segments exhibit gross fibrous thickening of the bowel wall, with serosal inflammation and congestion
      • Often skip areas of normal bowel are present between affected segments.
    • There may be
      • mesenteric “fat wrapping” (especially in small bowel).
      • Long or short stricture  
      • Sinus tract to walled serosal abscess and fistula to other bowel segments or adjacent structures  
    • The mucosa may exhibit discrete round ulcers on a background of normal mucosa.
      • There may be longitudinal ulcers (“bear-claw” or ‘train tracks” ulcers).
      • A cobblestone appearance is caused by linear ulcers running longitudinally and transversely across otherwise.
  • Microscopic pathology:
    • In areas of active disease, there is transmural inflammatory cell infiltrate composed of lymphocytes, macrophages, neutrophils and eosinophils.
    • There is marked mucosal architectural distortion with foci of cryptitis and crypt abscess.
    • The submucosa and muscularis propria are inflamed and fibrotic with scattered lymphoid aggregates, particularly in the strictured areas.
    • Deep fissuring ulcers are often present.
    • Noncaseating granulomas can be seen in all layers of the bowel wall and in mesenteric lymph nodes.

18

Idiopathic inflammatory bowel disease (IBD):
Comparison between Crohn’s disease and ulcerative colitis

  • Distribution
  • Stricture
  • Fistulae/sinuses
  • Inflammation
  • Ulcers
  • Lymphoid rxn
  • Granuloma
  • Pseudopolyp
  • Malignant risk

  • Distribution
    • CD: Skip lesions
    • UC: Diffuse
  • Stricture
    • CD: Variable/ common
    • UC: Late/ rare
  • Fistulae/sinuses
    • CD: Yes
    • UC: No
  • Inflammation
    • CD: Transmural
    • UC: Limited to mucosa
  • Ulcers
    • CD: Deep, linear
    • UC: Superficial
  • Lymphoid rxn
    • CD: Marked
    • UC: Mild
  • Granuloma
    • CD: Yes (50%)
    • UC: No
  • Pseudopolyp
    • CD: Yes
    • UC: Yes
  • Malignant risk
    • CD: Yes
    • UC: Yes

19

Colon polyps:
Hyperplastic polyps (p.72)

  • polyp
  • Hyperplastic polyps
    • frequency
    • appear grossly as/
    • frequently occur in/
    • Histologically, they are composed of/
    • considered/

  • polyp
    • any lesion projecting into the lumen of the bowel.
    • benign or malignant. 
  • Hyperplastic polyps
    • the most common type, accounting for 90 percent of colorectal polyp.
    • appear grossly as discrete, smooth, rounded mucosal elevations of 1 to 5 mm in size.
    • frequently occur in the rectosigmoid region, but can involve any part of the colon.
    • Histologically, they are composed of papillary tuft on the mucosal surface and sawtooth lumens in the crypts.
    •  considered benign and non-neoplastic before.
      • may be precancerous for large, numerous hyperplastic polyps in the proximal colon.

20

Colon polyps:
Adenomatous polyps (p.74-75)

  • can occur/
  • Grossly/
  • Microscopically/
  • two main histological subtypes of adenomas
  • The adenoma-carcinoma sequence

  • can occur at any age, but predominate in individuals over the age of 40 years.
  • Grossly, adenomas are pedunculated or sessile, which occur in all sizes and shapes.
  • Microscopically, the most common and reliable features are dysplastic nuclei composed of enlarged, elongated, pencil- or cigar-shaped nuclei arranged in a multilayered or pseudo-stratified manner.
    • Mucin depletion and dystrophic goblet cells are also commonly present.
  • two main histological subtypes of adenomas: tubular and villous adenomas.
  • The adenoma-carcinoma sequence
    • refers to a traditional view that colorectal malignancies develop from adenomatous polyps.
    • Since adenomatous polyps are considered precancerous lesions of adenocarcinoma they should be removed by endoscopic polypectomy or surgery with proper evaluation of the stalk.
    • The risk of cancer in adenoma increases with the size and grade of dysplasia and is also related to its histological subtypes.

21

Colon polyps:
Serrated adenomas:
Two major types of serrated polyp (p.79+81)

  • Traditional serrated adenoma (TSA)
    • contains/
    • constitute/
    • considered/
  • sessile serrated adenoma (SSA). 
    • Histologically/
    • characteristic features/
    • tendency
    • considered/

  • Traditional serrated adenoma (TSA)
    • contains
      • the architectural features of hyperplastic polyp and cytological features of adenomatous polyp.
      • foci of high-grade dysplasia
      •  of intramucosal carcinoma
    • constitute 1% to 2% of colon adenomas and is distributed throughout the colon.
    • considered as a variant of adenomatous polyp 
  • sessile serrated adenoma (SSA).
    • Histologically, SSA is similar to hyperplastic polyp,
    • characteristic features of the basal crypts, including dilatation, serration, branching, and horizontal orientation.
    • tendency to be right-sided, large (>1 cm), and sessile.
    • considered as the precursor of microsatellite instability (MSI) - positive colorectal cancer.

22

Colon polyps:
Juvenile polyps (p.83-84)

  • frequency and age
  • usually/
  • most frequent symptoms
  • most striking sign
  • grossly
  • Histologically, 

  • most common type of colorectal polyp in the childhood, especially before the age of 5 years.
    • may occur in persons of any age.
  • usually single and limited to the distal colon. 
  • Rectal bleeding is the most frequent symptoms, followed by the prolapse of the polyp through the rectum.
  • Autoamputation is the most striking sign.
  • grossly
    • round, pedunculated, and between 1 and 2 cm in diameter.
    • Erosion produces a red smooth surface.
    • On cross-section, mucin-filled retention cysts are usually visible.
    • The expanded stroma often appears gelatinous.
  • Histologically,
    • characterized by numerous cystic and dilated crypts, some filled with neutrophils and mucus.
    • intervening lamina propria is edematous and expanded by lymphocytes and plasma cells.

23

Colon polyps:
Peutz-Jeghers polyps and syndrome (p.87-88)

  • Peutz-Jeghers (PJ) polyps
    • ?
    • As an isolated lesion/
    • When it is a part of syndrome/
    • Clinical manifestations/
  • Peutz-Jeghers syndrome
    • characterized by/
    • inheritance
    • The gene is localized to/
    • 80% of clinically defined PJS families harbor/
    • considered/
    • associated with
  • The hallmark of a PJ polyp 

  • Peutz-Jeghers (PJ) polyps
    • are benign, hamartomatous polyps that may occur as an isolated lesion at any age or as part of Peutz-Jeghers syndrome.
    • As an isolated lesion it is most frequently encountered in the colon.
    • When it is a part of syndrome, the small bowel, especially the jejunum, is the main site of polyps.
    • Clinical manifestations include intussusception (47%), obstruction (42.8%), abdominal pain (23.4%), rectal bleeding (13.5%), and prolapse of the polyp (7.2%).
  • Peutz-Jeghers syndrome
    • characterized by gastrointestinal hamartomatous polyps and melanin spots on mucocutaneous surfaces, especially the lips, buccal mucosa, hands and feet.
    • The syndrome is of autosomal dominant inheritance with variable penetrance.
    • The gene is localized to the short arm of chromosome 19.
    • 80% of clinically defined PJS families harbor germline LKB1-inactivating mutation, thus defining the LKB1 serine/threonine kinase as a tumor suppressor protein.
    • considered a precancerous condition
    • associated with gastrointestinal tumors of the stomach, small bowel, colon, and pancreas as well as extra-intestinal tumors including sex cord tumor with annular tubules (SCTAT) and adenoma malignum (endocervical adenocarcinoma)
  • The hallmark of a PJ polyp
    • the intermixture of histologically normal mucosal elements (i.e., small bowel or colonic glandular mucosa) embedded in lamina propria, separated into lobules of fronds by branching bands of smooth muscle.

24

Colonic adenocarcinoma (p.90-92)

  • General features:
    • accounts for/
    • more common/
    • Multiple tumors/
    • The clinical presentation depends on whether the tumors develop in the right or left colon.
      • Cancers of the right colon
      • left-sided cancers
  • Gross features differ according to the side of colon involved.
    • differs according to/
    • A tumor that is present in the right side/
    • In the more distal portions (left side) of the colon/

  • General features:
    • accounts for 95% of malignant tumors of the colon.
    • more common in the distal colon.
    • Multiple tumors (synchronous and metachronous) occur in 3% of patients.
    • The clinical presentation depends on whether the tumors develop in the right or left colon.
      • Cancers of the right colon (cecum and ascending colon)
        • often flat or polypoid and the stool is soft in the right colon.
        • often remain clinically “silent” because they fail to cause obstruction or visible melena.
      • left-sided cancers in the rectosigmoid area often obstruct the intestinal lumen and cause bleeding.
  • Gross features differ according to the side of colon involved.
    • A tumor that is present in the right side is usually exophytic and cauliflower-like, with areas of hemorrhage and necrosis.
    • In the more distal portions (left side) of the colon, the tumor has napkin-ring configuration.

25

Colonic adenocarcinoma (p.93-96)

  • Histological features:
    • Most of the tumors
    • Mucin production
    • A signet-ring cell carcinoma
  • Staging
    • All systems classify tumors on/
  • Prognosis:
    • defined strictly by/
    • Additional factors which influence prognosis
    • the ploidy (DNA content) of the tumor
    • what has a poor prognosis.

  • Histological features:
    • Most of the tumors
      • well to moderately differentiated
      • resemble normal colonic mucosa.
    • Mucin production by the tumor is a variable.
    • A signet-ring cell carcinoma, similar to that found primarily in the stomach, may occur and carry a poor prognosis.
  • Staging:
    • All systems classify tumors on the basis of depth of invasion into the bowel wall and the presence or absence of lymph node metastasis.
  • Prognosis:
    • defined strictly by stage.
    • Additional factors which influence prognosis include tumor grade, tumor morphology, race, presence of lymphatic or vascular invasion, number of nodes with metastases, etc.
    • the ploidy (DNA content) of the tumor, as measured by flow cytometry, has shown to give independent prognostic information.
    • Aneuploid tumors and tumors with a high proliferative rate have a poor prognosis.